Interaction Information:

Comment

ExoU modulated PAI-1 release by both airway epithelial cells and macrophages. PAI-1 concentrations in supernatants from A549 epithelial respiratory cells and THP-1 macrophages infected with the ExoU-producing PA103 were significantly higher than concentrations detected in supernatants from control noninfected cells or from cells infected with the PA103 exoU mutant.

ExoU-induced PAI-1 overexpression was likely dependent on the PAF signaling system. The cell treatment with an anti-PAFR antibody prior to PA103 infection resulted in a significant reduction of both PAI-1 mRNA expression and PAI-1 concentration in cell culture supernatants, supporting the contribution of the PAF signaling system in the ExoU-induced antifibrinolytic environment in mice airways.

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